Dictyostelium development is initially characterized by the appearance of non-terminally differentiated prestalk and prespore cells. At culmination of development these cells, respectively, become the terminally differentiated vacuolized stalk and heat resistant spore cells. G protein/receptor response to secreted, extracellular cAMP is critical for these developmental events. We have now demonstrated that cAMP signal response for prestalk and prespore development differ, and that receptor function can ultimately act through both cell autonomous and non- autonomous pathways. In particular, stimulation of cAMP receptor, subtype 4 (CAR4) activates prestalk differentiation through an intracellular signalling cascade. Similarly, stimulation of CAR1 activates prespore differentiation but, CAR4, also acting in a cell autonomous manner in prespore cells, appears to be linked to an inhibitory pathway. In addition, a population of cells that express CAR4 also secretes a positive regulator of prespore differentiation CAR4 is not required for response to this secondary activator. The rZIP protein, that potentially acts downstream of CAR4 in prespore regulation, fractionates with nuclei and is capable of complex protein interaction through several specific domains. rZIP appears to sense and regulate a prespore signal perhaps mediated via the cAMP-dependent protein kinase (PKA). We have also identified a mutation that appears to be required for the differentiation of a population of prestalk cells that are responsible for activating the PKA gradient through the prespore region. Mutant cells differentiate into prespore cells poorly and do not form spores. The lipid droplet associated protein perilipin may play an important role in the differentiation of adipocytes. Preadipocyte cells that are blocked in their ability to accumulate perilipin arrest early after developmental stimulation. In contrast, already differentiated steroidogenic cells that lack perilipin may metabolize cholesterol ester droplets normally.